Abnormally fast heart rates are called tachycardias and pose the danger of progressing into ventricular fibrillation, which can be fatal. As used herein, the term “tachycardia” thus refers to a heart rate that is abnormally high or to an arrhythmia that includes a fast heart rate that is too high and potentially dangerous if permitted to continue.
When the ventricular chambers beat too quickly, the arrhythmia is referred to as ventricular tachycardia (known as VT). During ventricular tachycardia, the ventricles typically do not fill properly, and do not pump enough blood to the body. Symptoms of ventricular tachycardia include faintness, pounding in the chest, and loss of consciousness. These tachycardias may result from a number of different causes. For example, patients who have had myocardial infarctions, or other diseases that create scarring in the ventricular region of the heart, often develop monomorphic ventricular tachycardias, a type of tachycardia that originates from one ventricular focus, for example, from an area of scarring on the heart. This type of tachycardia is typically uniform and occurs at a regular rate. Faster instances of monomorphic ventricular tachycardias are often associated with hemodynamic compromise, whereas slower instances can be very stable.
When cells die in a myocardial infarct, they electrically uncouple from neighboring viable cells, making the infarct completely inexcitable. Intrinsic or paced wavefronts encountering such an obstacle generally split into two components that collide and recombine on the opposite side of the infarct. When tissue adjacent to the infarct excites prematurely, however, reentry can result if one of the wavefronts gets blocked in a region with reduced excitability. When blocking of one wavefront occurs, the other wavefront may be able to reenter the initial block site, causing a “reentrant circuit.” Action potentials will continually propagate around the infarct at a rate considerably faster than the heart's intrinsic rate—i.e., ventricular tachycardia. The reentrant circuit can be thought of as a conduction wavefront propagating along a tissue mass of approximately circular geometry.
This circular conduction will consist of a portion of refractory tissue and a portion of excitable tissue. To terminate the circuit, a pacing stimulus should be provided at the time and location when the tissue just comes out of refractoriness. If this occurs, the paced stimulation wavefront proceeds toward the advancing wavefront of the circuit, colliding with the wavefront and interrupting the circuit. Accordingly, the probability of antitachycardia pacing succeeding in terminating the ventricular tachycardia is related to the ability of the pacing stimulation wavefront to arrive at the location of the reentrant circuit (e.g., within a myocardium) in such a manner that the reentrant circuit is modified or interrupted.
There are several different pacing modalities that have been suggested for termination of tachycardia. The underlying principle is that if a pacing pulse stimulates the heart at least once shortly after a heartbeat, before the next naturally occurring heartbeat of tachycardic rate, the heart may successively revert to sinus rhythm.
Ventricular tachycardia is sometimes controlled by an implanted cardiac device that applies electrical therapies. For example, an implantable cardioverter-defibrillator (ICD) applies antitachycardia pacing (ATP) or an electric shock to the heart muscle after which a normal sinus rhythm often ensues. If an electric shock (i.e., cardioversion) is used to treat the ventricular tachycardia because the ventricular tachycardia has become recalcitrant, the electric shock may be in the form of specially timed pacemaker pulses (unfelt by the patient) or by high voltage shock. High voltage shocks, if required, are usually painful to the patient.
So, even though ATP is used to convert ventricular tachycardias into normal sinus rhythm, conventional ATP is not always completely successful at returning the heart to normal sinus rhythm. Consequently, cardioversion is used, but cardioversion is usually painful or at least unpleasant. Additionally, conventional ATP sometimes accelerates the rhythm to ventricular fibrillation. In women, for example, acceleration from ATP can occur in approximately 15% of ATP attempts. Thus, improved methods for increasing the success rate of ATP, for decreasing the time needed to convert the ventricular tachycardia to a normal sinus rhythm, and for reducing pain, are needed.